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66 Cards in this Set
- Front
- Back
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blood compostion
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a fluid connective tissue
- plasma + formed elements 1.erythrocyte (red blood cells or RBCs) 2.leukocyte (white blood cells or WBCs) 3,platelets (血小板） -Hematocrit (% of RBCs) [Male] 47%+- 5% [Female] 42%+- 5% |
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Centrifuge the blood sample
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plasma 55%
-Least dense component Formed elements 1.Buffy coat -leukocyte and platelets <1% 2.Erythrocytes 45% -most dense component |
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physical characteristics and Volume
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-Sticky, opaque fluid (metallic smell from iron)
-color scarlet (O2 rich) to dark red (O2 poor) -pH 7.35 -7.45 (strictly controlled - critical for life) -38C (100F) -〜8% of body weight -average volume [Male] 5-6 L [Females] 4-5 L |
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Function of Blood
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1.Distribution of
-O2 and nutrients to body cells -Metabolic wastes to the lungs and kidneys for elimination -hormones from endocrine organs to target oranges 2.Regulation of -body temperature by absorbing and distributing heat -Normal pH using buffers -Adequate fluid volume in the circulatory system 3.protection against -blood loss --plasma proteins and platelets initiate clot formation -infection --antibodies --complement proteins --WBCs defend against foreign invaders |
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blood plasma
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-straw colored
-90% water + over 100 solute --proteins are mostly produced by the liver --60% albumin: transporter, maintain osmotic pressure --36% globulins: alpha, beta, gamma --4% fibrinogen: clotting proteins -Nitrogenous by-products of metabolism -lactic acid, urea, creatinine, other ammonium wastes -Nutrients- glucose, carbohydrate, amino acids -Electrolytes- Na+, K+, Ca2+, Cl-, HCO3- -respiratory gases- O2, CO2 -hormones |
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Formed Elements
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-only WBCs are complete cells
-RBCs have no nuclei or organelles -Platelets are cell fragments -Most formed elements survive in the bloodstream for only are few days -most blood cells originate in bone marrow and do not divide once in the blood |
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Erythrocytes1
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-biconcave discs, anucleate, essentially no organelles
-Filled with hemoglobin (Hb) for gas transport -contain the plasma membrane protein spectrin and other proteins --provide flexibility to change shape as necessary --provide antioxidant enzyme -Are the major factor contributing to blood viscosity |
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Enthrocyte2
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-structural characteristics contribute to gas transport
--biconcave shape: huge surface area relative to volume (30% more surface area) -->97% hemoglobin (not contain water) -- No mitochondria; ATP production is anaerobic: no O2 is used in generation of ATP -A superb example of complementarity of structure and function |
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Enthyrocyte3 function
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-RBCs are dedicate to respiratory gas transport
-hemoglobin binds reversibly with oxygen -hemoglobin structure --protein globin: tow alpha and two beta chains --heme pigment bonded to each globin chain -iron atom in each heme can bind to one O2 molecules -Each Hb molecule can transport 4 O2 molecules -Each RBC has 250 million Hb molecules --1 billion molecules O2 per RBC |
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Hemoglobin (Hb)1
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-O2 loading in the lungs
--produces oxyhemoglobin (ruby red) -O2 unloading in the tissues --produces deoxyhemoglobin or reduced hemoglobin (dark red) -Co2 loading in the tissues --produces carbaminohemoglobin (carries 20% of CO2 in the blood- binding to an AA, not to the hemo) |
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Hematopoiesis (hemopoiesis)
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-blood cell formation
--occurs in red bone marrow of axial skeleton, girdles and proximal epiphyses of humerus and femur -Hemocytoblasts (hematopoietic stem cells) --Give rise to all formed elements --hormones and growth factors push the cell toward a specific pathway of blood cell development -new blood cells enter blood sinusoids |
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Erythropoiesis 1
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-erythropoiesis: red blood cell production (3-15 days)
--A hemocytoblast is transformed into a proerythroblast --proerythroblasts develop into early erythroblasts --phases in development 1.Ribosome synthesis 2.Hemoglobin accumulation 3.Ejection of the nucleus & formation of reticulocytes -reticulocytes then become mature erythrocyte |
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Erythropoiesis 2
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A hemocytoblast (transformed)
↓ proerythroblasts (develop) ↓ early erythroblasts ↓ Ribosome synthesis ↓ hemoglobin accumulation ↓ ejectiont the nucleus fromation of reticulocyte ↓ Erythrocytes |
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Regulation of erythropoiesis
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- too few→tissue hypoxia
--hemorrhage or ↑RBC destruction →↓RBC numbers --insufficient hemoglobin (iron deficiency) --↓ availability of O2 (high altitudes) -Too many RBCs ↑blood viscosity -Balance between RBC production & destruction depends on --hormonal controls --adequate supplies of iron, amino acids, & vitamin B |
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Hormonal control of erythropoiesis
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-Erythropoietin (EPO)
--Direct stimulus for erythropoiesis --Released by the kidneys in response to hypoxia -effects of EPO --more rapid maturation of committed bone marrow cells --↑ circulating reticulocyte count in 1-2 days -testosterone also enhances EPO production, resulting in higher RBC counts in males |
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Erythropoietin mechanism for regulating erythropoiesis
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1 stimulues: hypoxia due to
-↓ RBC count= ↓ hemoglobin = ↓ availability of O2 2 Kideny >& liver release eryhtropoietin 3 Erythropoetin stimulates red bone marrow 4 Enhanced eryhtopoiesis ↑ RBC count 5 O2 Carying ability of blood ↑ |
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Dietary requirements for erythropoiesis
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-Nutrients- amino acids, lipids,& carbohydrates
-iron --stored in Hb (65%), the liver, spleen, and bone marrrow --Stored in cell as ferritin & hemosiderin --transported loosely bound to the protein transferrin (free iron is toxic) --small amounts lost daily: sweat, faces, urine, menstrual flow -Vitamin B12 and folic acid- necessary for DNA synthesis for cell division |
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Fate and destruction of erythrocytes
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-life span: 100-120 days
-Old RBCs become fragile, and Hb begins to degenerate -Macrophages engulf dying RBCs in the spleen -heme and globin are separated --iron is salvaged for reuse --heme is degraded to yellow the pigment bilirubin --liver secretes bilirubin (in bile) into the intestines --Dgraded pigment leaves the body in faces as stercobilin --globin is metabolized into amino acids |
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Erythrocyte disorders
Anemia: |
: blood has abnormally low O2- carrying capacity
-a sign rather than a disease itself -blood O2 levels cannot support normal metabolism --accompanied by fatigue, paleness, shortness of breath and chills |
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causes and type of Anemia 1
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1 insufficient erythrocytes
-hemorrhagic anemia: acute or chronic loss of blood -Hemolytic anemia: RBCs rupture prematurely -Aplastic anemia: destruction or inhibition of red bone marrow |
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causes and type of Anemia 2
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2.Low hemoglobin content
-iron-deficiency anemia --secondary result of hemorrhagic anemia or --inadequate intake of iron-containing foods or --impaired iron absorption -Pernicious anemia --deficiency of Vitamin B12 --Lack of intrinsic factor needed for absorpiton of B12 --Treated by intramuscular injection of B12 or application of Nscobal |
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causes and type of Anemia3
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Abnormal hemoglobin
-thalassemias --absent or faulty globin chain -RBCs are thin, delicate, & deficient in hemoglobin -Sickle-cell anemia --defective gene codes for abnormal hemoglobin (HbS) --CauseRBCs to become sickle shaped in low-oxygen situations |
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Erythrocyte Disorders
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-polycythemia: excess of RBCs that ↑ blood viscosity
[Results from:] --polycythemia vera- bone marrow cancer --hematocrit as high as 80% -secondary polycythemia- when less O2 is available (high altitude, smokers) or when EPO production ↑ -blood doping- RBC2 removed, EPO naturally stimulated, RBCs reinjected = high (RBCs) |
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Leukocyte (WBCs)
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-Make up < 1% pf total blood volume
-Can leave capillaries via diapedesis -move through tissue spaces by ameboid motion & positive chemotaxis -Leukocytosis: WBC count over 11.000/mmm3 --Normal response to bacterial or viral invasion |
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WBCs: Granulocytes or agranulocyte
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-Granulocytes: neurophils, eosinophils, & Basophils
--Cytoplasmic granules stain specifically with Wright's stain --Langer and shorter-lived than RBCs --Lobed nuclei --Phagocytic -Agranulocytes: lymphocytes & monocytes --Lack visible cytoplasmic granules --Have spherical or kidney shaped nuclei |
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Neurophils
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most numerous WBSs
-Polymorphonuclear leukocytes (PMNs) -Fine granules take up both acidic &basic dytes -Give the cytophasmatic a lilac color -Granules contain hydrolytic enzyme or defensins -Very phagocytic-"bactereria slayers" |
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Eosinophils
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-Red-staining, bilobed nuclei
-red to crimson (acidphoilic) carse, lysosome- like granules -Digest parasitic worms that are too large to be phagocyytized -Modulators of the immune response |
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Basophils
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-rarest WBCs
-Large, purple-black (basophilic) granules contain histamine --histamine: an inflammatory chemical that acts as a vasodilator & attracts other WBCS to inflamed sites -Are functionally similar to mast cells |
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Lymphocytes
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-Large, dark-purple, circular nuclei with a thin rim of blue cytoplasm
-mostly in lymphoid tissue; few circulate in the blood -crucial to immunity -2 types 1. T cell act against virus- infected cells 2.B cells give rise to plasma cells which produce antibodies |
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Monocytes
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-The largest luekocytes
-Abundant pale-blue cytoplasm -Dark purple-staining, U- or kidney- shaped nuclei -Leave circulation, enter tissues, & differentiate into macrphages --actively phagocytic cells; crucial against viruses, intracellular bacterial parasite,& chronic infections -activate lymphocytes to mount an immune response |
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Leukopoiesis
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-Production of WBCs
-Stimulated by chemical messengers from bone marrow & mature WBCs --Interieukins (ex:IL1,IL2) --colony-stimulating factors (CSFs) named for the WBC type they stimulate (ex: granulocyte-CSF stimulates granulocyte) -All leukocytes originate from hemocytoblasts -Many hematopoietic hormones (EPO, CSFs) are used clinically to stimulate bone marrow and the immune response (Cancer, AIDS patients) |
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Leukocyte formation
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(Stem cells) Hemocytoblasts differeniate into myeloid stem cells & lymphoid stem cells
(Committed cells) -Myeloid stem cells become myeloblasts or monoblasts -Lymphoid stem cells become lymphoblasts |
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Leukocyte disorders
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-leuopenia: abnormally low WBC count- drug induced
-Leukemias: --cancerous conditions involving WBCs --Named according to the abnormal WBC clone involved =myelocytic leukemia involves myeloblasts =Lymphocytic leukemia involves lymphocytes -A cute leukemia involves blast-type cells and primarily affects children -Chronic leukemia is more prevalent in older people |
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Leukemia
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-bone marrow totally occupied with cancerous leukocytes
-Immature nonfunctional WBCs in the bloodsteam -Death caused by internal hemorrhage & overwhelming infections -treatment include irradiation, antileukemic drugs, and stem cell transplants |
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Platelets
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-small fragments of megakaryocytes
-formation is regulated by thrombopoietin -blue-staining outer region, purple granules -granules contain serotonin, Ca2+, enzymes, ADP, & platelet- derived growth factor (PDGF) -Form a temporary platelet plug that helps seal breaks in blood vessles -Circulating platelets are kept inactive and mobile by NO & prostacyclin from endothelial cells of blood vessels |
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Hemostasis
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-Fast series of reactions for stoppage of bleeding
1.vascular spasm: smooth muscle contracts, causing vasoconstriction 2. Platelet plug formation: injury to lining of vessel exposes collagen fibers; platelets adhere -Platelets release chemicals that make near by platelets sticky; platelet plug forms 3.Coagulation (blood clotting): fibrin forms a mesh that traps red blood cells & platelets, forming the clot |
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1. Vascular spasm
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-vasoconstriction of damaged blood vessel
-triggers --direct injury --chemicals released by endothelial cells and platelets --Pain reflexes |
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2. Platelet plug formation (〜1 min)
-positive feedback cycle -At site of blood vessel injury, platelets |
-stick to exposed collagen fibers with the help of von Willerbrand factor, a plasma protein
-Swell, become spiked & sticky, & release their contents --ADP cause more platelets to stick & release their contents --serotonin & thromboxane A2 enhance vascular spasm & mor e platelet aggregation |
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3. Coagulation (3-6 min)
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-a set of reactions in which blood is transformed from a liquid to a gel
-reinforces the platelet plug with fibrin threads -3 phases of coagulation 1. prothrombin activator is formed (intrinsic & extrinsic pathways) 2.Prothrombin is converted into thrombin 3. thrombin catalyzes the joining of fibrinogen to form a fibrin mesh |
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Coagulation phase1
Tow pathways to prothrombin Activator |
-Initiated by either the intrinsic or extrinsic pathway (usually both)
--triggered by tissue-damaging events --involves a series of procoagulants --each pathway cascades toward factor X -Factor X complexes with Ca2+, PF3 & factor V to form prothrombin activator [Intrinsic pathway] -is triggered by negatively charged surfaces (activated platelets, collagen, glass) -Uses factors present within the blood (intrinsic) [Extrinsic pathway] -is triggers by exposure to tissue factor (TF) or factor III (an extrinsic factor) -Bypasses several steps of the intrinsic pathway, so is faster |
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Coagulation phase2
Pathway to thrombin |
-prothrombin activator catalyzes the transformation of prothrobin to the active enzyme thrombin
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coagulation phase3
common pathway to the fibrin mesh |
-thrombin converts soluble fibrinogen into fibrin
-Fibrin strands form the structural basis of a clot -Fibrin causes plasma to become a gel-like trap for formed elements -thrombin (w/ Ca2+) activates factor XIII which: --cross-links fibrin --strengthens & stabilizes the clot |
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clot retraction
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-actin & myosin in platelets contract within 30-60 minutes
-platelets pull on the fibin strands, squeezing serum from the clot |
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clot repair
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-platelet- deriverd growth factor (PDGF) stimulates division of smooth muscle cells & fibroblasts to rebuild blood vessel wall
-Vascular endothelial growth factor (VEGF) stimulates endothelial cells to multiply & restore the endothelial lining |
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Fibrinolysis
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-begins within tow days
-plasminogen in clot is coverted to plasmin by tissue plasminogen activator (tPA), factor XII & thrombin -plasmin is a fibrin-digesting enzyme [Factors limiting clot growth or formation] -Tow homeostatic mechanisms prevent clots from becoming large 1. Swift removal & dilution of clotting factors 2.Inhibition of activated clotting factors |
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2.inhibition of clotting factors
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-most thrombine is bound to fibrin threads, & prevented from action elsewhere
-Antithrombin III, protein C, & heparin inactivate thrombin & other procoagulants -heparin, another anticoagulant, also inhibits thrombin activity |
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Factors preventing undesirable clotting
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pletelet adhesion is prevented by
-smooth endothelial lining of blood vessels -Antithrombic substances nitric oxide & prostacyclin secreted by endothelial cells -Vitamin E quinine which acts as potent anticoagulant |
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Disorders of Hemostasis
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1. thromboembolytic disorder: undesirable clot formation
2.Bleeding disorders: abnormalities that prevent normal clot formation |
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1.Thromboembolytic conditons
(Hemostasis) |
[thrombus]: clot that develops & persists in an unbroken blood vessle
-may block circulation, leading to tissue death [Embolus]: a thromus freely floating in the blood steam -pulmonary emboli impair the ability of the body to obtain oxygen -cerebral emboli can cause strokes [prevented by] -aspirin= antiprostaglandin that inhibits thromboxane A2 -Heparin= anticagulant used clinically for pre & postoperative cardiac care -Warfgarin= used for these prone to atrial fibrillation |
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Disseminated intravascular coagulation (DIC)
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-Eidespread clotting blocks intact blood vessels
-severe bleeding occurs bc residual blood unable to clot -Most common in pregnancy, septicemia, or incompatible blood transfusions |
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2.bleeding disorders
(Hemostasis) |
[Thrombocytopenia]: deficient number of circulating platelets
-petechiae appear due to spntaneous, widespread hemorrhage -due to suppression or destruction of bone marrow (ex, malignancy, radiation) -platelet count < 50000/mm3 is diagnostic -treated w/ transfusion of concentrated platelets [impaired liver function] -inability to synthesize procoagulants -causes include vitamin K deficiency, hepatities, and cirrhosis -Liver disease can also prevent the liver from producing blile, impairing fat & vitamin K absorption |
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2.bleeding disorder
(Hemostasis) |
hemophilias include several similar hereditary bleeding disorders
-Hemophilia A: most common type (77% of all cases); due to a dificiency of factor Vlll -Hemophilia B: deficiency of factor IX -Hemophilia C: mild type; deficiency of factor XI symptoms include prolonged bleeding, especially into joint cavities theated with plasma transfusions & injection of missing factors |
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Transfusions
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-whole-blood transfusions are used when blood loss is substantial
-packed red cells (plasma removed) are used to restore oxygen-carrying capacity -transfusion of incompatible blood can be fetal |
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Human blood groups
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*RBC membranes bear 30 types glycoprotein antigens that are
-perceived as foreign if transfused blood is mismatched -unique to each individual -promoters of agglutination are called agglutinogens *Presence or absence of each antigen is used to classify blood cells into different groups |
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Blood groups
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-humans have 30 varieties of naturally occurring RBC antigens
-antigens of the ABO & Rh blood groups cause vigorous transfusion reactions -other blood groups (MNS, Duffy, Kell, & Lewis) are usually weak agglutinogens *agglutinogens (〜antigens)+agglutinins(antiblodies) =agglutination |
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Rh blood groups
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-there are 45 different Rh agglutinogens (RH factors)
-C,D,&E most common -Rh+ indicates presence of D -Anti-RH antibodies are not spontaneously formed in Rh- individual -A second exposure to Rh+ blood will result in a typical transfusion reaction |
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Homeostatic imbalance: hemolytic disease of the new born (or erythroblastosis fetalis)
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-Rh- mother becomes sensitized when exposure to Rh+ blood causes her body to synthesize anti Rh antibodies
-Anti-Rh antibodies cross the placenta & distroy the RBCs of an Rh+ baby -the baby can be treated w/ prebirth transfusions & exchange transfusions after birth -RhoGAM serum containing anti-Rh can prevent the Rh- mother from becoming sensitized |
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transfusion reactions
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*occur if mismatched blood is infused
*Donor's cells -are attacked by the recipient's plasma agglutinins -agglutinate & clog small vessels -rupture & release free hemoglobin into the bloodsteam [result in] -diminished oxygen-carrying capacity -hemoglobin in kidney tubules & renal failure -self-transfusions (autologous tissue donation) |
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Blood typing
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-when serum containing anti-A or anti-B agglutinins is added to blood, agglutination will occur between the agglutinin & the corresponding agglutinogens
-positive reactions indicate agglutination |
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Blood type A
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[RBC agglutinogens] A
[serum reaction]Anti-A+, anti-B- [plasma antibodies(agglutinins)] B [possible transfusion] A+=A+,A-,O+,O- A-=A-,O- |
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Blood type B
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[RBC agglutinogens] B
[serum reaction]Anti-A-, anti-B+ [plasma antibodies(agglutinins)] A [possible transfusion] B+=B+,B-,O+,O- B-=B-,O- |
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Blood type AB
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[RBC agglutinogens] AB
[serum reaction] anti-A+, anti-B+ [plasma antibodies(agglutinins)] None [possible transfusion] AB+=AB+,AB-,A+,A-,B+,B,-O+,O- *universal receiver AB-=AB-,A-, B-,O- |
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Blood type O
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[RBC agglutinogens] None
[serum reaction] None [plasma antibodies(agglutinins)] anti-A, anti-B [possible transfusion] O+=O+,O- O-=O- (universal donor) |
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restoring blood volume
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*death from shock may result from low blood volume
*volume must be replaced immediately w/ -Normal saline or multiple-electrolyte solution that mimics plasma electrolyte composition -plasma expanders (ex purified human serum albumin, hetastarch, & dextran) --mimic osmotic properties of albumin -more expensive & may cause significant complication |
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diagnostic blood test
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-hematocrit
-blood glucose tests -microscopic examination reveals variations in size & shape of RBCs, indication of anemias -differential WBC count -prothrombin time & platelet counts assess hemostasis -SMAC, a blood chemistry profile -Complete blood count (CBC) |
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development aspects
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-fetal blood cells from in the fetal yolk sac, liver,& spleen
-red bone marrow is the primary hematopoietic area by the seventh month -blood cells develop from mesenchymal cells called blood islands -the fetus forms HbF, which has a higher affinity for O2 than hemoglobin A formed after birth -blood diseases of aging --chronic leukemias, anemias, clotting disorders --usually precipitated by disorders of the heart, blood vessls, & immune system |
